Author + information
- Received September 28, 1992
- Revision received April 12, 1993
- Accepted April 21, 1993
- Published online November 1, 1993.
- Raul D. Mitrani, MDa,b,1,
- Lawrence S. Klein, MD, FACCa,b,
- William M. Miles, MD, FACCa,b,
- F.Kevin Hackett, MDa,b,
- Robert W. Burt, MDa,b,
- Henry N. Wellman, MDa,b and
- Douglas P. Zipes, MD, FACC∗,a,b
- ↵∗Address for correspondence: Dr. Douglas P. Zipes, Krannert Institute of Cardiology, 1111 West Tenth Street, Indianapolis, Indiana 46202-4800.
Objective. The aim of this study was to determine whether patients with ventricular arrhythmias in the absence of coronary artery disease also have abnormalities in sympathetic innervation.
Background. We have previously shown by cardiac sympathetic scintigraphy using iodine-123-metasiodobenzylguanidine (I-123-MIBG) that patients with ventricular tachycardia after myocardial infarction have regional cardiac sympathetic denervation. It is not known whether patients with ventricular tachycardia in the absence of coronary artery disease also have regional cardiac sympathetic denervation.
Method. We performed cardiac I-123-MIBG and thallium-201 single-photon emission computed tomographic (SPECT) scans at rest in 18 patients (mean age 47 ± 18 years) with cardiomyopathy (n = 6), left ventricular hypertrophy (n = 1), valvular disease (n = 2) or a structurally normal heart (n = 9) who presented with monomorphic (n = 15) or polymorphic (n = 3) ventricular tachycardia. These scans were compared with scans in 12 control patients without ventricular tachycardia (mean age 30 ± 17 years) who had cardiomyopathy (n = 3) or a structurally normal heart (n = 9). Cardiac sympathetic denervation was defined as myocardial areas having thallium uptake with reduced or absent I-123-MIBG uptake.
Results. Twelve (67%) of 18 patients with ventricular tachycardia had regional cardiac sympathetic denervatlon compared with 1 (8%) of 12 patients who did not have ventricular tachycardia (p = 0.002). In the nine patients with a structurally normal heart and ventricular tachycardia, five (55%) patients had regional cardiac sympathetic denervatlon compared with zero of nine control patients with a structurally normal heart (p = 0.029). Five patients underwent right ventricular radiofrequency ablation for ventricular tachycardia, and sympathetic denervatton was adjacent to the ablation site in one of these patients.
Conclusions. Patients with ventricular tachycardia in the absence of coronary artery disease have abnormal cardiac sympathetic innervation detectable by cardiac sympathetic scintigraphy. The rote of regional cardiac sympathetic denervatton in arrhythmogenesis remains to be determined.
↵1 Dr. Mitrani is a recipient of North American Society of Pacing and Electrophysiology Fellowship, July 1991–June 1992.
☆ This study was supported in part by the Herman C. Krannert Fund, Indianapolis; Grants HL-42370 and HL-07182 from the National Heart, Lung, and Blood Institute of the National Institutes of Health, Bethesda Maryland; United States Public Health Service, Washington, DC; The Attorney General of Indiana Public Health Trust, Indianapolis; American Heart Association, Indiana Affiliate, Indianapolis. It was presented as part of the Young Investigator Awards Competition at the Annual North American Society of Pacing and Electrophysiology Meeting, Chicago, May 1992.
- Received September 28, 1992.
- Revision received April 12, 1993.
- Accepted April 21, 1993.